Involvement of Rac GTPase activation in phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to ICAM-1
(2011) In Biochemical and Biophysical Research Communications 406(2). p.273-277- Abstract
Increasing evidence indicates that phospholipid oxidation plays important roles in atherosclerosis. Here, we investigated the involvement of Rho-family GTPases inphosphatidylcholine hydroperoxide (PCOOH)-induced THP-1 cell adhesion to ICAM-1. Isoprenoid depletion by fluvastatin and geranylgeranyltransferase inhibition by GGTI-286 suppressed PCOOH-induced cell adhesion to ICAM-1 and F-actin-rich membrane protrusion formation. Pull-down assays demonstrated the activation of Rac1 and Rac2 in PCOOH-treated cells. Pan-Rho-family GTPase inhibitor Clostridium difficile toxin B, Rac-specific inhibitor NSC23776, and RNA interference of the Rac isoforms suppressed the cell adhesion. These findings indicate the involvement of Rac GTPase activation... (More)
Increasing evidence indicates that phospholipid oxidation plays important roles in atherosclerosis. Here, we investigated the involvement of Rho-family GTPases inphosphatidylcholine hydroperoxide (PCOOH)-induced THP-1 cell adhesion to ICAM-1. Isoprenoid depletion by fluvastatin and geranylgeranyltransferase inhibition by GGTI-286 suppressed PCOOH-induced cell adhesion to ICAM-1 and F-actin-rich membrane protrusion formation. Pull-down assays demonstrated the activation of Rac1 and Rac2 in PCOOH-treated cells. Pan-Rho-family GTPase inhibitor Clostridium difficile toxin B, Rac-specific inhibitor NSC23776, and RNA interference of the Rac isoforms suppressed the cell adhesion. These findings indicate the involvement of Rac GTPase activation in PCOOH-induced cell adhesion to ICAM-1 via actin reorganization.
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- author
- Asai, Akira ; Okajima, Fumitaka ; Nakajima, Yasushi ; Nagao, Mototsugu LU ; Nakagawa, Kiyotaka ; Miyazawa, Teruo and Oikawa, Shinichi
- publishing date
- 2011-03-11
- type
- Contribution to journal
- publication status
- published
- keywords
- Actin, Cell adhesion, Monocyte, Phosphatidylcholine hydroperoxide, Phospholipid oxidation, Rac
- in
- Biochemical and Biophysical Research Communications
- volume
- 406
- issue
- 2
- pages
- 5 pages
- publisher
- Elsevier
- external identifiers
-
- scopus:79952450625
- ISSN
- 0006-291X
- DOI
- 10.1016/j.bbrc.2011.02.032
- language
- English
- LU publication?
- no
- id
- db223ece-ddea-444f-86f0-9488449fcd09
- date added to LUP
- 2017-08-23 20:05:39
- date last changed
- 2022-01-30 22:14:55
@article{db223ece-ddea-444f-86f0-9488449fcd09, abstract = {{<p>Increasing evidence indicates that phospholipid oxidation plays important roles in atherosclerosis. Here, we investigated the involvement of Rho-family GTPases inphosphatidylcholine hydroperoxide (PCOOH)-induced THP-1 cell adhesion to ICAM-1. Isoprenoid depletion by fluvastatin and geranylgeranyltransferase inhibition by GGTI-286 suppressed PCOOH-induced cell adhesion to ICAM-1 and F-actin-rich membrane protrusion formation. Pull-down assays demonstrated the activation of Rac1 and Rac2 in PCOOH-treated cells. Pan-Rho-family GTPase inhibitor Clostridium difficile toxin B, Rac-specific inhibitor NSC23776, and RNA interference of the Rac isoforms suppressed the cell adhesion. These findings indicate the involvement of Rac GTPase activation in PCOOH-induced cell adhesion to ICAM-1 via actin reorganization.</p>}}, author = {{Asai, Akira and Okajima, Fumitaka and Nakajima, Yasushi and Nagao, Mototsugu and Nakagawa, Kiyotaka and Miyazawa, Teruo and Oikawa, Shinichi}}, issn = {{0006-291X}}, keywords = {{Actin; Cell adhesion; Monocyte; Phosphatidylcholine hydroperoxide; Phospholipid oxidation; Rac}}, language = {{eng}}, month = {{03}}, number = {{2}}, pages = {{273--277}}, publisher = {{Elsevier}}, series = {{Biochemical and Biophysical Research Communications}}, title = {{Involvement of Rac GTPase activation in phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to ICAM-1}}, url = {{http://dx.doi.org/10.1016/j.bbrc.2011.02.032}}, doi = {{10.1016/j.bbrc.2011.02.032}}, volume = {{406}}, year = {{2011}}, }